The vertebrate immune system has evolved in response to the threat posed by viruses. A number of viruses have evolved gene products for subverting specific elements of the immune system. Nonspecific immune mechanisms can be triggered by cellular sensing of viral invasion, viral destruction of cells, recognition of infected cells by natural killer (NK) cells, or direct interaction of complement with virions. Plasmacytoid dendritic cells (pDCs) are bone marrow-derived cells that are the source for most of the initial wave of type I interferons (IFNs) induced by many viruses. These cells reside in the T-cell regions of the spleen and lymph nodes and can be activated by noninfectious forms of viruses. Signals transduced through recognition of pattern recognition receptors (PRRs) at the onset of innate responses critically impact the development of adaptive immune responses. NK cells can directly interfere with viral reproduction by releasing cytokines with antiviral activity or by lysing virus-infected cells. Macrophages play a role in the destruction of antibodycoated virions, via Fc receptor-mediated internalization of immune complexes into lysosomes. The role of neutrophils in viral immunity is very poorly defined, even though neutrophils, like macrophages, are highly abundant phagocytic cells with Fc receptors and are recruited in large numbers to sites of viral infection. The most important result of T-cell receptor (TCR) stimulation of naive T cells is the increase in the transcription of interleukin-2 (IL-2) and the IL-2 receptor.